Chicken CH25H inhibits ALV-J replication by promoting cellular autophagy

文献类型： 外文期刊

第一作者： Xie, Tingting

作者： Xie, Tingting;Feng, Min;Zhang, Xi;Li, Xiaoqi;Mo, Guodong;Zhang, Xiquan;Xie, Tingting;Zhang, Xi;Li, Xiaoqi;Mo, Guodong;Zhang, Xiquan;Xie, Tingting;Zhang, Xi;Li, Xiaoqi;Mo, Guodong;Zhang, Xiquan;Shi, Meiqing

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关键词： chicken; ALV-J; CH25H; ISG; autophagy

期刊名称：FRONTIERS IN IMMUNOLOGY （ 影响因子：7.3； 五年影响因子：8.0 ）

ISSN： 1664-3224

年卷期： 2023 年 14 卷

页码：

收录情况： SCI

摘要： Autophagy plays an important role in host antiviral defense. The avian leukosis virus subgroup J (ALV-J) has been shown to inhibit autophagy while promoting viral replication. The underlying autophagic mechanisms, however, are unknown. Cholesterol 25-hydroxylase (CH25H) is a conserved interferon-stimulated gene, which converts cholesterol to a soluble antiviral factor, 25-hydroxycholesterol (25HC). In this study, we further investigated the autophagic mechanism of CH25H resistance to ALV-J in chicken embryonic fibroblast cell lines (DF1). Our results found that overexpression of CH25H and treatment with 25HC promoted the autophagic markers microtubule-associated protein 1 light chain 3 II (LC3II) and autophagy-related gene 5(ATG5), while decreased autophagy substrate p62/SQSTM1 (p62) expression in ALV-J infection DF-1 cells. Induction of cellular autophagy also reduces the levels of ALV-J gp85 and p27. ALV-J infection, on the other hand, suppresses autophagic marker protein LC3II expression. These findings suggest that CH25H-induced autophagy is a host defense mechanism that aids in ALV-J replication inhibition. In particular, CH25H interacts with CHMP4B and inhibits ALV-J infection in DF-1 cells by promoting autophagy, revealing a novel mechanism by which CH25H inhibits ALV-J infection. Although the underlying mechanisms are not completely understood, CH25H and 25HC are the first to show inhibiting ALV-J infection via autophagy.

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